Brain abscess A complication of cystic fibrosis in adults.

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NOTES AND LETTERS
Neurological Complications
of Thyrotoxicosis in
the Elderly
Tim Florin, MB,"
and Ronald S. Walls, MB, DPhil (0xon)T
The recent report of a patient in thyrotoxic storm with corticospinal tract disease that improved with appropriate antithyroid drugs and plasmapheresis IS] prompts us to record a
further case. Our patient differed from others reported in
that she had treated pernicious anemia. She too evidenced
neurological symptoms that reversed on treatment of her
hyperthyroid state.
The patient is a 77-year-old woman who developed progressive weakness and inability to walk over two months. For
the previous 15 years she had been treated for pernicious
anemia with regular monthly vitamin Blz injections (1 mg).
Neither peripheral neuropathy nor subacute combined degeneration had been documented prior to institution of BLL
therapy. The patient was fully compliant with treatment. O n
admission she had muscle wasting and weakness, more
marked proximally and predominantly in the lower limbs,
with hypotonia, diminished knee jerks, absent ankle jerks,
and bilateral Babinski's signs. There was impaired vibration,
joint position, and light touch sensation in the hands and the
lower limbs, but pain and temperature sensation were not
affected. The patient was anxious, had a multinodular goiter,
and was in atrial fibrillation, but there were no other signs of
thyrotoxicosis. Serum biochemistry results and thyrotropinreleasing hormone stimulation indicated hyperthyroidism
with poor peripheral conversion of T4 to Ti. Findings of
nerve conduction studies and electromyography were consistent with neuropathy. Sereum B12 and red blood cell folate
levels were normal. Results of Schilling's test and gastroscopy
with biopsy were consistent with pernicious anemia. Parietal
cell antibodies were detected, but antibodies to intrinsic factor, thyroglobulin, thyroid microsomes, and acetylcholine receptor were absent. Following treatment with carbimazole
and iodine 131, her gait, power, and nerve conduction improved and her sensation and Babinski's signs returned to
normal, suggesting an association between myeloneuropathy
and hyperthyroidism.
The association of thyrotoxicosis and proximal myopathy is
well recognized, but that of thyrotoxicosis and other
neurological syndromes is less well known. Peripheral neuropathy [ 3 ] , pyramidal tract involvement [I, 2, 5 , 61,and
posterolateral myelopathy (1 patient) 141 have been reported
in association with thyrotoxicosis. The neurological deficits in
our patient may have resulted from the extra demands placed
by hyperthyroidism o n the metabolism of nerves already
compromised from vitamin B12 deficiency prior to initiation
of therapy for pernicious anemia. Thyrotoxicosis could in
this way have unmasked a previously subclinical myeloneuropathy. In the only other known report describing an
association between hyperthyroidism and posterolateral myelopathy 141, the patient was floridly thyrotoxic, whereas hyperthyroidism was masked in our patient. Me wish to emphasize that thyroid function should be evaluated in cases of
608
otherwise unexplained neurological syndromes in the elderly,
because hyperthyroidism is often clinically masked in this age
group.
"Department of Medicine
Royal Prince Alfved Hospital
Camperdown
TDepartment of Medicine
University of Sydney
Concord Hospital
Concord
Nezu South Wales, Australia
References
1. Bulens C: Remission of spastic paraplegia, dementia and optic
neuropathy. Arch Neurol 38:669-670, 198 1
2 . Garcia CA, Fleming RH: Reversible corticospinal tract disease
due to hyperthyroidism. Arch Neurol 34:647-648, 1977
3. McComas AJ, Sica REP, McNabb AR, er ak Neuropathy In thyrotoxicosis. N Engl J Med 289:219-220, 1973
4. Melamed E, Berman M, Lavy S: Posterolareral myelopathy associated with thyrotoxicosis. N Engl J Med 293.798-799, 1975
5. Newcomer J, Haire W, Hartman CR: Coma and thyrotoxicosis.
Ann Neurol 14:689-690, 1383
6. Ravera JJ, Cervino JM, Fernandez G, et al: Two cases of Graves'
disease with signs of a pyramidal lesion: improvemrnr in
neurologic signs during treatment with anrirhyroid drugs. J Clin
Endocrinol 203764380, 1960
Brain Abscess:
A Complication of
Cystic Fibrosis in Adults
Charles S. Rabkin, MD," and Martin J. Blaser, MD"t
Brain abscess is a common sequel to infection in the lung but
seldom accompanies the pulmonary infections of cystic
fibrosis [11.
A 19-year-old man with cystic fibrosis was admitted to the
hospital for evaluation of his first seizure. H e had had cystic
fibrosis since infancy, with a relatively stable course until
three months prior to admission, when he had had his first
episode of pneumonia. He had been treated as an outpatient
with trimethoprim and sulfamethoxazole (Bactrim DS) and
had improved. Five days prior to admission he developed a
right frontal headache, which worsened after coughing. This
was followed by several brief episodes of vertigo, nausea, and
light-headedness. He also noted transient sensations of deji
w. The symptoms persisted, and five days later he had a
tonic-clonic convulsion. H e denied fevers, chills, sweats, stiff
neck, photophobia, difficulty in thinking, earache, nasal
stuffiness, or rhinorrhea.
O n examination the patient appeared comfortable. His examination showed no abnormalities except for a respiratory
rate of 28 per minute and increased anteroposterior diameter
of the chest, with rare coarse rhonchi on forced expiration.
He had digital clubbing but no cyanosis or edema. The
neurological findings were normal.
Characteristics of Reported Patients with Cystic Fibrosis and Brain Abscess
Patient
No.
1
2
Age
(yrl
Status of
Pulmonary
Disease
Duffner and
Cohen,
1979 131
21
Bronchiec-
Fischer er
al, 19?9
(41
17
Report
taSlS
Cor p d monale
Presentation
Duration of
Symptoms
before
Diagnosis
(days)
Fever
Present
Seizure,
increasing
coma
No
Focal neurological
findings,
headache,
vomiting
No
Cercbrospinal Fluid
Cell Count
(4)
Antibiotics
Operarion
Bacteriology
Outcome
2 leukocytes
Oxaciliin, genta
micin, chloramphenicol;
changed to
penicilln,
chloramphenicol
Oxxillin, carbenicillin,
chloramphenicol
Yes; twice
Puptustwpf o(urns (after
5 days of
rherapy)
Seizure
disorder
Yes
Prpfo~trepro-
Never
awoke
postoperat1vely;
died 3 wk
later
(after
1 day of
therapy );
Pruteus and
Aprpfh
m1-cu.i
(post-
3
Fischer et
al, 1979
24
Clubbing
141
4
s
Fischer et
al, 1979
[41
19
Sherman e t
al, 1980
r51
20
Fever,
headache,
nausea,
vomiting,
meningism
Yes
No
Bronchiec-
Not on adnusrion,
yes at
24 hr
Headache and
seizures
Chloramphenicol; changed
ro penicillin
Yes; 3
rimes
mortem)
Viridans
streptococci
(afrer I day
of therapy)
Chloramphenicol, erythromycin;
changed to
penicillin;
changed to
erythromycin
Carbenicillin,
gentamicin,
chloramphenicol, oxacillin
Yes, with
later
ventriculoatrid
shunring
Ungroupable
aerobic
streptococci
(afrer 7 days
of therapy)
N o neuro-
Yes
Sterile (after
13 days of
therapy)
No neurological
deficit
No
...
No neuroIoglcal
deficit
Yes
Sterile (after
12 davs of
therapy)
N o neuroloeical
deiicit
95%
BronchiecVomiting,
tasis, clubhemiarbing
opia
lasIS
40,800
leukocytes,
POIYmorpho
nuclear
. .
7 leuko-
cytes,
57%
poky-
No neurological
deficit
logical
deficit
morpho
nuclear
6
Ayres and
Kinsella,
1980 [ l l
22
Cor pulmonale
7
Present
report
19
Clubbing
Seizures and
focal neurological findings
Headache,
vertigo,
seizure
No
Computed tomographic scan of the head showed a 2.5 X
1.5 x 1.5 cm medial right temporal lobe enhancing lesion
with a central lucency that displaced adjacent arteries on angiography. The paranasal sinuses contained chronic inflammatory changes.
The patient was treated with chloramphenicol and penicillin, 15 million units a day for twelve days, after which a wellencapsulated mass was removed from the temporal lobe. No
organisms were identifiable, and all cultures were negative.
The patient recovered neurologically but died four months
later of respiratory failure. Postmortem examination revealed
no evidence of active brain infection.
The most serious consequence of cystic fibrosis is chronic
and recurrent pulmonary infection, leading to lung destruction, and respiratory insufficiency. Infection outside the respiratory system is a rarity C2). This relative protection from
dissemination of infection may be explained by several factors. The use of antimicrobial agents is responsible, because
in the preantibiotic era fatal septicemia often complicated
Ampicillin, Aucloxacillin,
metroniduole
Chloramphenicol, penicillin
staphylococcal pneumonia in children with cystic fibrosis C2).
General immunological function in patients with cystic
fibrosis is intact [Z].
The literature reveals only six previous cases of brain abscess in patients with cystic fibrosis 11, 3-51, all in adults
(Table). The absence of pediatric cases suggests some morbid
developments in long-standing disease necessary before susceptibility to brain abscess is established. Advanced anatomical lung disease can be surmised in each of the six reported
patients with brain abscess, as well as in our patient, from the
presence of bronchiectasis, clubbing, and cor pulmonale. As
supportive therapies improve, patients with cystic fibrosis are
living longer and thus surviving with more severe lung abnormalities [b). In the four cystic fibrosis abscesses in which
bacteria were isolated (see the Table), aerobic or anaerobic
streptococci were found. Including our patient, only one
(14%) of seven died.
Most abscesses secondary to cystic fibrosis have been
managed with a regimen of wide-spectrum antibiotics fol-
Notes and Letters 609
lowed by surgical excision. We suggest the use of chloramphenicol and penicillin for empirical treatment when cystic
fibrosis is present. The one reported patient with brain abscess and cystic fibrosis who received medical therapy alone
did well IS]. Patients who are improving on a regimen of
antibiotic therapy and whose radiographic lesions show regression should be considered for treatment with antibiotics
alone to resolution of their disease. Operation would be reserved for those abscesses increasing in size or threatening
crucial structures by extension or mass effect.
'Department of Medicine
University of Colorado School o j Medicine and
the ilnfectious Disease Section
Veterans Administration Medical Center
Denver, CO 80220
References
1. Ayeres J, Kinsella H: Multiple cerebral abscesses in an adult with
cystic fibrosis. Br J Dis Chest 76:99-101, 1982
2. DiSant'Agnese PA, Dans PB: Research in cystic fibrosis. N Engl J
Med 295:597-602, 1976
3. Duffner PK, Cohen ME: Cystic fibrosis with brain abscess. Arch
Neurol 3627-28, 1979
4. Fischer EG, Shwachman H, Wespie JG: Brain abscess and cystic
fibrosis. J Pediatr 95:385-388, 1979
5. Sherman JM, Oranstein DM, Stern RC: Brain abscess and cystic
fibrosis. J Pediarr 96952, 1980
6. Shwachrnan H, Kowalski M, Khaw KT: Cystic fibrosis: a new
outlook. Medicine 56:129-149, 1977
Outcome in Neonates
with Seizures: Are Chronic
Anticonvulsants Necessary?
Peter Gal, PharmD," Martha K. Sharpless, MD,'r§
and Henry R. Boer, MD$B
The article by Bergman and colleagues [ l ) prompted us to
review the outcome in 35 neonates treated in our intensive
care nursery between October 1979 and November 1982
and followed for 13 to 50 months (mean, 28 months). Although seizure classification was not recorded for many neonates, most infants had generalized tonic-clonic seizures or
focal or multifocal partial seizures. Asphyxia was implicated
as the sole or partial cause in 27 patients. Other causes implicated included intraventricular hemorrhage ( 5 cases), sepsisimeningitis ( 4 cases), and metabolic disturbances (2 cases).
The neurological outcomes are summarized in the Table.
Seizures persisted or recurred in 3 children, all of whom had
severe brain damage, due either to asphyxia (2) or to herpes
encephalitis (1). All seizures were managed with phenobarbital, and 6 patients required additional anticonvulsants, including 2 of 3 patients needing continued anticonvulsant
therapy. Treatment was continued until patients were clinically stable for 3 to 5 days and the apparent cause of the
seizure had disappeared. Two patients required continued
anticonvulsant therapy because seizures recurred when the
610 Annals of Neurology Vol 15 No 6 June 1984
Outcome in 35 Neonates Treatedfor Seizure in the
lntensive Care Nursery in Relation to Gestational Age
Neurological Status
Gestational Age
31 wk or less
32-36 wk
37 wk or more
Total
Normal
4
5
14
23
Mild
Impairment
3
Moderatel
Severe
Impairment
1
2
1
1
4"
5
7
"Seizures occurred in 3 patients.
drugs were withheld. One patient was discharged on no
medication regimen but at 7 months developed seizures that
were not controlled with high doses of phenobarbital. This
patient had required only phenobarbital to control the
neonatal seizures.
Although the numbers are small, the neurological outcome
in our neonates appears somewhat better than that reported
by Bergman and colleagues [l]. Most patients with neonatal
seizures did not require long-term anticonvulsanr therapy.
Only 857 of the population in the report by Bergman and coworkers had unexpected, frequent seizure recurrences, and
approximately the same percentage of our patients required
long-term anticonvulsant therapy. Patients with mild or no
neurological problems were at low risk: none of our 28 patients and only 5 of the 68 patients of Bergman and coworkers in this category had later seizures. In contrast, seizures recurred or persisted in 4 3 2 of our patients and 31%
of those of Bergman and associates with severe neurological
sequelae.
These findings support the impression that most neonates
do not need long-term anticonvulsant therapy for seizures.
One should attempt to discontinue these drugs while patients
are still in the intensive care nursery [ 3 ] . Only the presence
of severe sequelae appears to predict seizure recurrences. We
stress this point because a recent survey of neonatologists and
neurologists [2] found that over 85cZ of respondents
routinely continued therapy for 2 months or longer and 40%
required a normal electroencephalogram in order to stop
anticonvulsant treatment. Even in patients in whom seizures
returned after discontinuation of anticonvulsants, control
could be regained by reinstitution of therapy.
'Area Health Education Center and iPediztric Teac-bingService.
and $Neonatologist
Moses H . Cone Memorial Hospital
Greensboro, N C 27401-1020 and
"School of Pharmacy and $School of Medicine, Diziic-ion 01
Pediatrics
University of North Carolina at Chapel Hill
Chapel Hill, N C 27514
References
1. Bergman I , Painter MJ, Hirsch RP, et al: Outcome in neonates
with convulsions treated in an intensive care unit. Ann Nrurol
1 4 6 4 2 4 4 7 , 1983